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跛足鸭还是凶猛野兽?少突胶质细胞在多发性硬化症中的作用。

Lame ducks or fierce creatures? The role of oligodendrocytes in multiple sclerosis.

作者信息

Zeis T, Schaeren-Wiemers N

机构信息

Neurobiology, Department of Biomedicine, University Hospital Basel, Pharmacenter 7007, Klingelbergstrasse 50/70, CH-4056 Basel, Switzerland.

出版信息

J Mol Neurosci. 2008 May;35(1):91-100. doi: 10.1007/s12031-008-9042-1. Epub 2008 Feb 16.

Abstract

In the pathogenesis of multiple sclerosis (MS), oligodendrocytes and its myelin sheaths are thought to be the primary target of destruction. The mechanism leading to oligodendrocyte injury and demyelination is still elusive. Oligodendrocytes are maintaining up to 50 internodes of myelin, which is an extraordinary metabolic demand. This makes them one of the most vulnerable cell types in the central nervous system (CNS), and even small insults can lead to oligodendrocyte impairment, demyelination, and axonal dysfunction. For this reason, oligodendrocytes are viewed as more or less the "lame ducks" of the CNS who can easily become victims. However, recent data demonstrate that this perception possibly needs to be revised. The latest data suggest that oligodendrocytes may also act as "fierce creatures," influencing the surrounding cells in many ways to preserve its own, as well as their function, allowing sustained functionality of the CNS upon an attack. In this review, the concept of "reactive or activated oligodendrocyte" is introduced, describing alterations in oligodendrocytes which are either protective mechanisms allowing survival in otherwise lethal environment or influence and possibly modulate the ongoing inflammation. Although "harnessed", oligodendrocytes might actively modulate and shape their environment and be part of the immune privilege of the brain.

摘要

在多发性硬化症(MS)的发病机制中,少突胶质细胞及其髓鞘被认为是主要的破坏靶点。导致少突胶质细胞损伤和脱髓鞘的机制仍不清楚。少突胶质细胞维持着多达50个髓鞘节段,这是一种非凡的代谢需求。这使它们成为中枢神经系统(CNS)中最脆弱的细胞类型之一,即使是轻微的损伤也会导致少突胶质细胞损伤、脱髓鞘和轴突功能障碍。因此,少突胶质细胞或多或少被视为中枢神经系统中容易成为受害者的“跛脚鸭”。然而,最近的数据表明,这种看法可能需要修正。最新数据表明,少突胶质细胞也可能表现为“凶猛的生物”,通过多种方式影响周围细胞以保护自身及其功能,使中枢神经系统在受到攻击时仍能持续发挥功能。在这篇综述中,引入了“反应性或活化少突胶质细胞”的概念,描述了少突胶质细胞的改变,这些改变要么是在致命环境中允许存活的保护机制,要么是影响并可能调节正在进行的炎症反应。尽管少突胶质细胞是“被利用的”,但它们可能会积极调节和塑造其环境,并成为大脑免疫特权的一部分。

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